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MRCPsych Part B - Al-Rashid Hospital > Liaison Psychiatry > Flashcards

Liaison Psychiatry Flashcards

1
Q

What is Premenstrual syndrome (PMS)?

A

Collection of psychological and somatic sx occurring during the luteal phase of menstruation.

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2
Q

How many patients with PMS suffer from severe PMS?

A

5%

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3
Q

How many women suffer from severe PMS?

A

3-8%

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4
Q

% of women with severe PMS who have a comorbid mood disorder?

A

30-70%

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5
Q

What are women with PMDD at higher risk of?

A

Postnatal depression

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6
Q

Where in ICD is Premenstrual tension syndrome?

A

Diseases of the Genitourinary tract

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7
Q

Where was PMS classified in DSM IV?

A

Under depressive disorder not otherwise specific

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8
Q

Where is PMS in DSM V?

A

As a diagnosis

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9
Q

Which sx of PMS are not seen in depression?

A

Breast pain

Bloating

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10
Q

At least 1 of which sx must be present for a diagnosis of PMDD for DSM V

A

Depressed mood
Marked anxiety
Marked affective lability
Marked anger or irritabiity

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11
Q

Duration of sx for diagnosis of PMDD for DSM V

A

In most menstrual cycles during past year, at least 5 of the 11 sx including one of the first 4 should be present

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12
Q

What are the other sx for PMDD under DSM V aside from the first 4

A

Anhedonia
Subjective sense of difficulity concentrating
Lethargy
Marked change in appetite or specific food craving
Hypersomnia/insomnia
Subjective sense of being overwhelmed/loss of control
Physical sx

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13
Q

When must sx be present for PMDD diagnosis in DSM V

A

Must be present most of the time during lat week of luteal phase
Must begin to remit within few days of onset of menstrual flow
Must be absent in the week after menses

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14
Q

Functional criteria for PMDD dx under DSM V

A

Sx must markedly interfere with work, school, social activities or relationships

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15
Q

Exclusion criteria for PMDD

A

Sx cannot be an exacerbation of another disorder such as depression

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16
Q

How must criteria be confirmed for PMDD under DSM V?

A

By prospective daily ratings for at least 2 consecutive menstrual cycles

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17
Q

Pattern for symptoms in PMS

A

During each cycle, sx last for a few days to up to 2 weeks.

Peak is 2 days before menses.

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18
Q

Hypothesis of pathology underlying PMS

A

Increased sensitivity to normal fluctuation of gonadal hormones.

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19
Q

How do we know that serotonin has a role in PMS?

A

Serotonin-enhancing treatments reduce PMS symptoms.

Impairment in serotonin transmission provokes sx.

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20
Q

What does imaging suggest re the pathology of PMS?

A

May be a role of GABA due to its interaction between progesterone metabolites and GABA-A receptors

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21
Q

Treatment of mild PMS

A

Lifestyle changes
CBT
Exercise/diet

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22
Q

Treatment for severe PMS

A

SSRIs

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23
Q

SSRI response rate for PMS

A

60-90% compared with 30-40% with placebo

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24
Q

Effective medications for PMS

A 
Fluoxetine or Sertraline (best)
Citalopram
Escitalopram
Clomipramine
Venlfaxine
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25
Q

Which non-SSRIs can be used for PMS?

A

Clomipramine

Venlafaxine

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26
Q

Which SSRIs can be used for PMS?

A

Fluoxetine
Sertraline
Citalopram
Escitalopram

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27
Q

Impact of SSRIs on PMS?

A

Reduce mood and somatic sx

Improve QoL and social functioning

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28
Q

Most effective drug for PMS

A

Fluoxetine

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29
Q

What other dosing regime can be used for PMS?

A

Intermittent dosing during luteal phase; 2 weeks prior to menses.

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30
Q

Odds ratio of SSRI treatment for PMS

A

6.91 in favour of SSRIs compared with placebo

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31
Q

Difference in sx reduction between continuous and intermittent dosing for PMS?

A

No difference

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32
Q

Disadvantages of intermittent dosing for PMS?

A

Lower efficacy for somatic sx

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33
Q

Advantages of intermittent dosing for PMS

A

More effective than continuous
Cheaper
Less withdrawal due to SEs

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34
Q

When do SSRIs become effective for PMS?

A

WIthin a few days

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35
Q

Difference in side effects if SSRIs used for depression vs. PMS

A

In PMS lower frequency of sexual side effects and no reports of akathisia or increased suicidal ideation

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36
Q

Which other medications can be used (with caution) in PMS?

A

Alprazolam in premenstrual insomnia and anxiety

Hormonal treatment

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37
Q

How does hormonal treatment work in PMS?

A

Suppresses ovulation

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38
Q

Which hormonal treatments can be used for PMS?

A

Long-acting GnRH agonist, oestrogen

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39
Q

When should hormonal treatment be considered for PMS?

A

Only as last resort

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40
Q

Possible consequences of hormonal treatment for PMS

A

Introducing early menopause

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41
Q

Remission rates of PMS

A

Low on cessation of treatment

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42
Q

How many patients with coronary heart disease have comorbid depression?

A

20%

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43
Q

What type of interventions can reduce depression in patients with coronary artery disease?

A

Psychological & behavioural

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44
Q

Risk of patients with persistent depression who also have coronary artery disease?

A

Increased cardiac risk

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45
Q

Studies in patients with coronary artery disease and depression

A

Enhancing Recovery in Coronary Heart Disease (ENRICHD) for CBT
Myocardial Infarction and Depression Intervention Trial (MIND-IT)
Canadian Cardiac Randomization Evaluation of Antidepressant and Psychotherapy Efficacy (CREATE) for interpersonal therapy
COPES - problem-solving therapy trial
Women’s Heart Study - CBT based stress management

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46
Q

What do ENRICHD and MIND-IT show?

A

CBT only has modest effects on depression and neither improve survival.

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47
Q

What is the largest randomised trial evaluating use of antidepressants on depressed patients with heart disease?

A

Sertraline Antidepressant Heart Attack Randomized Trial (SADHART)

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48
Q

Structure of SADHART

A

Compared Sertraline v placebo in 16 week trial

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49
Q

Results of SADHART

A

No difference in safety (LVEF, premature ventricular contractions, QTc prolongation)
Nonsignificant reduction in endpoint (MI or CHD death) in Sertraline group

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50
Q

What did SADHART show re impact of Sertraline on depression?

A

Little difference in depression status after 24 weeks treatment
Effect of Sertraline greater in patients with severe and recurrent depression

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51
Q

Prevalence of depression in CCF patients

A

21.5% (2-3 times higher than general population)

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52
Q

What is higher prevalence of depression in CCF associated with?

A

Females

Higher NYHA functional class

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53
Q

Relative risk of mortality in patients with CCF who are depressed

A

2:1 compared to risk in non-depressed CCF patients

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54
Q

What does severe depression in CCF increase rates of?

A

Clinical events
Rehospitalisation
General health care use

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55
Q

Psychiatric sx in hyperthyroidism

A 
Generalised anxiety
Depression
Irritability
Hypomania
Cognitive dysfunction
Mania in severe thyrotoxicosis
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56
Q

M:F ratio of hypothyroidism

A

1:6

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57
Q

Psychiatric sx of hypothyroidism

A

Depression
Cognitive dysfunction
Psychosis in severe cases

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58
Q

What is subclinical hypothyroidism a risk factor for?

A

Depression

Rapid cycling in Bipolar

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59
Q

Sx at mild-moderate (10-14) hyperparathyroidism?

A

Depression
Apathy
Irritability
Lack of initiative

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60
Q

Sx at severe (>14) hyperparathyroidism

A

Delirious with psychosis
Catatonia
Lethargy progressing to coma

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61
Q

Sx in mild hypoparathyroidism

A

Anxiety
Paresthaesias
Irritability
Emotional Lability

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62
Q

Sx in severe hypoparathyroidism

A

Mania
Psychosis
Tetany
Seizures

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63
Q

Most common cause of Cushings Syndrome

A

Exogenous steroids

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64
Q

What causes Cushings disease?

A

ACH secretion from pituitary tumour

Corticosteroid secretion from adrenal adenoma

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65
Q

Physical sx of Cushings syndrome

A 
Diabetes
Hypertension
Muscle weakness
Obesity
Osteopenia
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66
Q

Psychiatric sx of Cushings syndrome

A 
Depression (most common)
Anxiety
Hypomania/mania
Psychosis
Cognitive dysfunction
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67
Q

Which type of steroid is more likely to produce mania?

A

Exogeneous

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68
Q

Psychiatric sx of Addisons

A 
Apathy
Anhedonia
Fatigue
Depression
Anorexia
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69
Q

Which sx are present in Addisons but not in depression?

A

Nausea, vomiting

Skin changes 0 dark pigmentation

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70
Q

What causes Acromegaly?

A

Excess growth hormone

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71
Q

Psychiatric sx of Acromegaly

A

Mood lability
Personality change
Depression

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72
Q

How can Acromegaly cause psychosis?

A

With treatment of Bromocriptine - dopamine agonist

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73
Q

Cause of Phaechromocytoma?

A

Catecholamine-secreting tumour

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74
Q

Physical sx of Phaechromocytoma>

A

Tachycardia
Labile hypertension
Headache/sweating
Episodic palpitations

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75
Q

How is Pheochromoctyoma screened?

A

Urinary catecholamines - Vanillyl mandelic acid, metanephrines

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76
Q

Best diagnostic test for Pheochromoctyoma?

A

Plasma metanephrine level

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77
Q

Rates of depression in patients with Diabetes

A

2-3 times more common compared to general population

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78
Q

Correlation between Depression and Diabetes

A

Poorer glycaemic control

Increased diabetic complication

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79
Q

Which psychiatric disorders have increased prevalence of TII DM?

A

Bipolar
Schizophrenia (2-4 times higher)
Severe depression

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80
Q

How can Diabetes lead to cognitive dysfunction?

A

Frequent hyperglycaemic episodes result in cerebral micro and macrovascular damage

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81
Q

Prevalence of depression in those with advanced cancer

A

5-15%

82
Q

Which sx are not useful in diagnosing depression in those with advanced cancer?

A

Somatic sx

83
Q

What is a useful criterion for depression in those with advanced cancer?

A

Pervasive global anhedonia

84
Q

Drug treatments for depression in palliative care

A

SSRI
Low dose Amitriptyline
Lofepramine
Rapid-acting psychostimulants e.g. Dexamphetamine/methylphenidate

85
Q

When should Amitriptyline be avoided in palliative care?

A

High risk of delirium

86
Q

When is Amitriptyline helpful in palliative care?

A

Neuropathic pain

87
Q

Prevalence of delirium in cancer in-patients?

A

44%

88
Q

Prevalence of delirium in patients shortly before death

A

62%

89
Q

Impact of diazepam use in end stage renal disease?

A

The metabolite desmethyldiazepam may accumulate, causing excessive sediation

90
Q

Impact of Lorazepam in end stage renal disease

A

Half life increased from 8-25 hours to 32-65 hours.

91
Q

By how much should lorazepam dose be reduced in low level of renal function?

A

By 50%

92
Q

Which antidepressants can be used at normal dose in renal impairment?

A

Imipramine
Amitriptyline
Fluoxetine
Fluvoxamine

93
Q

Which antidepressant should not be used in renal impairment?

A

Sertraline

94
Q

Which medications should be reduced in renal impairment and the elderly?

A

Half dose of Citalopram

Reduced dose in Paroxetine

95
Q

Which antipsychotic should be avoided in renal impairment?

A

Amisulpride

96
Q

Which antipsychotic does not require dose reduction in renal impairment?

A

Haloperidol - unless excessive sedation or hypotension occur

97
Q

Dosing of Amisulpride in renal failure if no other option

A

Alternate day dosing or dose reduction

98
Q

Impact of Risperidone in renal impairment

A

Active metabolite 9-hydroxy-risperidone is excreted in urine so eliminatino half life is prolonged

99
Q

When does uraemic encephalopathy occur?

A

When eGFR falls to 10% of normal

100
Q

Sx of uraemic encephalopathy

A 
Cognitive dysfunction
Psychomotor activity 
Change in personality
Vomiting
Restlessness
Myoclonus
Coma
101
Q

What is dialysis disequilibrium syndrome?

A

Temporary clinical disorder that may occur during first few days of dialysis.

102
Q

Who is dialysis disequilibrium syndrome more common in?

A

Younger patients

Pre-existing neurological problems

103
Q

Sx of dialysis disequilibrium syndrome?

A 
Headache
Restlessness
Nausea/vomiting
HTN
Tremor
Disorientation
Seizures
104
Q

What are most of the sx of dialysis disequilibrium syndrome a result of?

A

Cerebral Oedema

105
Q

What causes Lyme disease?

A

Borrelia burgdorgeri transmitted via wooden tick bite which lives on deers.

106
Q

Signs of Lyme disease

A

Red spot develops around location, and develop a central clearing called erythema migrans within 4 weeks.

107
Q

How many patients with erythema migrans develop neuroborreliases?

A

15%

108
Q

What is neuoborreliases?

A

Lyme disease where CNS is affected

109
Q

Sx of Lyme disease

A

Back pain worse at night
Facial numbness
Facial palsy

110
Q

Where is Lyme disease common?

A

North America

111
Q

Sx of late-stage Lyme disease

A 
Memory impairment
Word-finding problems
Visual/spatial processing impairment
Slowed processing of information
Psychosis
Seizures
Violent behaviour
112
Q

Psychiatric sx of SLE

A

Depression
Anxiety
Psychosis (Rare)

113
Q

Physical sx of SLE

A

Chronic, remitting-relapsing course of febrile illness, butterfly rash, inflammation of joints, kidney and serosa

114
Q

In which patients with SLE is butterfly rash common?

A

Middle-aged women

115
Q

What characterises SLE?

A

Anti-nuclear antibodies

116
Q

CNS manifestations of SLE

A 
Peripheral neuropathy
Grand mal seizures
Chorea and choreoathetosis
Cognitive impairment
Severe headaches
Stroke
B Cell Lymphoma
Limbic-encephalitis type picture
117
Q

Sx of Insulinoma

A

Recurrent headache
Lethargy
Diplopia/blurred vision - with exercise/fasting
Psychosis/depression

118
Q

What is Neurosarcoidosis?

A

Idiopathic granulomas in various tissue - mainly lungs and mediastinal node.
May affect CNS - mainly CN.

119
Q

Sx of neurosarcoidosis

A

Bilateral facial palsy
Depression - 20%
Psychosis
Erythema nodosium

120
Q

Blood test results in Neurosarcoidosis

A

Raised ACE levels due to macrophage activity

121
Q

Treatment of Neurosarcoidosis

A

Immunosuppression

122
Q

What happens in Metachromatic Leucodystrophy (MLD)?

A

Impairment of development of myelin sheath.

123
Q

Cause of MLD

A

Genetic defecs of enzyme arylsulfatase A.

124
Q

Forms of MLD

A

Late infantile
Juvenile
Adult

125
Q

What is the most common form of MLD?

A

Late infantile

126
Q

Signs of late infantile MLD?

A 
Children have difficulting walking after first year of life
Muscle wasting/weakness
Muscle rigidity
Developmental delays
Progressive loss of vision leading to blindness
Convulsions
Impaired swallowing
Paralysis
Dementia
127
Q

Outcome of late infantile MLD

A

Most children die by age of 5

128
Q

Onset of juvenile MLD

A

3-10 years of age

129
Q

Sx of juvenile MLD

A

Impaired school performance
Mental deterioration
Dementia
Slower progression of sx of late infantile MLD

130
Q

When does adult form of MLD begin?

A

> 16 years of age

131
Q

Sx of adult form of MLD

A

Progressive dementia or psychiatric disorder
Mental deterioration
Depression

132
Q

How many patients with adolscent-onset MLD have schizophrenia-like psychosis?

A

60%

133
Q

What is Neuroacanthocytosis?

A

Genetically heterogenous neurologic disorder characterised with acanthocytosis.

134
Q

Sx of Neuroacanthocytosis?

A 
Movement disorders/ataxia
Personality changes
Cognitive deterioration
Axonal neuropathy
Seizures -tonic-clonic
Subcortial dementia
135
Q

What is acanthocytosis?

A

10-30% of patients erythrocytes having a star-like appearance with projections.

136
Q

Gait of those with neuroacanthocytosis?

A

Lurching with long strides

Quick, involunary knee flexion

137
Q

Age of onset of MS

A

20-40

138
Q

Lifetime risk of MS in the UK

A

1:8000

139
Q

Gender disparity in MS

A

Twice as common in women

140
Q

Geographical distribution of MS

A

Greater frequency as distance from equator increases

141
Q

Pathology of MS

A

Multiple demyelinating lesions with predilection for optic nerves, cerebellum, brainstem and spinal cord.

142
Q

How many people with MS have a steady progression of disability with no remission?

A

5-10%

143
Q

How many patients with MS have a relapsing-remitting course?

A

20-30%

144
Q

How many patients with MS have a progressive deterioration following a number of relapses and remissions?

A

60%

145
Q

Treatment for MS

A

Steroids

Glatiramer acetate

146
Q

How does Glatiramer acetate work for MS?

A

Neuroprotective

Immunomodulator

147
Q

When is Glatiramer acetate used in MS?

A

Reduces frequency of relapses in relapsing-remitting MS

148
Q

Trade name of Clatiramer acetate?

A

Copaxone

149
Q

Dose of Glatiramer acetate?

A

20mg OD s/c

150
Q

Lifetime prevalence of depressive sx in MS

A

40-50% - 3x higher than general population

151
Q

What is depression in MS linked with?

A

Poorer cognitive function
Poor compliance with treatment
Lower QoL

152
Q

What can cause drug-induced low mood in MS?

A

Steroids
Baclofen
Dantrolene
Tizanidine

153
Q

Brain abnormalities between MS and depression?

A

None

154
Q

Treatment used for depression in MS?

A

Desipramine
SSRI
ECT

155
Q

Risk of ECT use in MS

A

20% risk of triggering relapse of MS

156
Q

What must be done before ECT is used for depression in MS?

A

MRI to look for presence of active brain lesions - risk factor for MS relapse

157
Q

Suicide rates of people with MS

A

3% over 6 year period

15% over 16 years

158
Q

Drug-induced mania causes in MS

A

Steroids
Baclofen
Dantrolene
Tizanidine

159
Q

What is Tizanidine?

A

Central muscle relaxant

160
Q

How many patients with MS on steroids develop mild to moderate mania?

A

33%

161
Q

Which patients with MS on steroids are more likely to develop hypomania?

A

FHx of affective disorder/alcoholism

Premorbid history of affective disorder/alcoholism

162
Q

Link between Psychosis and MS

A

Patients with psychosis and mania who have MS have plaques distributed in bilateral temporal horn areas

163
Q

Psychiatric sx of MS

A 
Depression
Psychosis
Mania
Pathological laughing and crying syndrome/pseudobulbar affect
Cognitive Impairment
164
Q

Treatment for pathological crying/laughing in MS

A 
75mg Amitroptyline OD
Amantadine
Levodopa
Fluoxetine 
Sertraline
Citalopram
165
Q

Impact of Amitriptyline on pathological crying/laughing in MS?

A

66% of patients had improvement in sx

166
Q

What type of cognitive impairment is seen in MS?

A

Subcortical pattern

167
Q

Is MMSE useful to identify cognitive impairment in MS?

A

No

168
Q

Treatment for cognitive impairment in MS?

A

Donepezil

169
Q

Prevalence of post-stroke depression?

A

35%

170
Q

Which type of stroke has higher incidence of depression?

A

Subcortial

Infarcts of basal ganglia - especially left hemisphere.

171
Q

What type of stroke has high incidence of anxiety?

A

Cortical

172
Q

Prevalence of post-stroke anxiety?

A

25%

173
Q

Prevalence of apathy without depression in stroke?

A

20%

174
Q

Prevalence of emotional incontinence in stroke?

A

20%

175
Q

Prevalence of catastrophic reaction in stroke?

A

20%

176
Q

Mean duration of post-stroke depression?

A

34 weeks

177
Q

Screening guidelines for depression and anxiety in stroke

A

Screen in first month after stroke.
Confirm emotionalism by simple questions.
If one mood disorder is present, assess for others

178
Q

Treatment for mild-moderate post-stroke depression

A

Increase social interaction
Exercise
Psychosocial intervention

179
Q

Treatment for severe post-stroke depression

A

Antidepressants

Monitor effectiveness

180
Q

How long should antidepressants be used for post-stroke depression if good initial effect

A

At least 4 months

181
Q

Which antidepressants have good evidence for post-stroke depression?

A

Fluoxetine

Citalopram

182
Q

Frequency of depression in epilepsy

A

30-50%

183
Q

Frequency of panic disorder in epilepsy

A

20%

184
Q

Frequency of psychosis in epilepsy

A

3-7%

185
Q

Which type of epilepsy is depression most common in?

A

TLE

186
Q

Risk of suicide in patients with epilepsy

A

10-15%

187
Q

Mortality rate if epilepsy and depressed

A

25x higher than general population

188
Q

First line treatment of depression in epilepsy

A

SSRIs - may reduce seizure threshold

189
Q

Which type of epilepsy is psychosis more common in

A

Partial epilepsies

190
Q

Risk factors of psychosis in epilepsy

A

Role of mesial temporal and extratemporal damage

191
Q

When is episodic psychosis most common in epilepsy?

A

Post-ictal

192
Q

What is more common in post-ictal psychosis than in functional psychosis?

A

Visual hallucinations

193
Q

Which psychotropic can cause psychosis?

A

Vigabatrin

194
Q

Which antipsychotics are less epileptogenic?

A

Sulpride

Haloperidol

195
Q

What are pseudoseizures linked with?

A

Past psychiatric hx
Somatisation
Social stressors
Childhood abuse

196
Q

Prolactin levels in seizures

A

Increased after epileptic seizures but should be taken within 15 mins of seizure

197
Q

Prevalence of depression in Parkinsons

A

40-50%

198
Q

Prevalence of hypomania/euphoria in Parkinsons

A

2%/10%

199
Q

Prevalence of anxiety in Parkinsons

A

50-65%

200
Q

Prevalence of Psychosis in Parkinsons

A

40% - drug-related

201
Q

Prevalence of cognitive impairment in Parkinsons

A

19% if no dementia

25-40% if dementia

MRCPsych Part B - Al-Rashid Hospital (64 decks)

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